Pathogenesis (development of disease)
In terms of their triggers, two forms of food allergy are distinguished:
- Primary food allergy: due to gastrointestinal sensitization to predominantly stable food allergens (e.g., milk and chicken egg whites, soy, wheat, peanut, and tree nuts)Anaphylactic shock due to food allergy (most common trigger of severe anaphylaxis in childhood)
- Secondary food allergy: sensitization to aeroallergens, such as pollen, and resulting cross-allergy to often unstable food allergens (90% of cases).
Food allergy can be triggered by several factors. Thus, in some allergy sufferers not a food or ingredient alone, but in a certain combination with other foods or ingredients leads to clinical complaints (multifactorial genesis). An important role is also played by the simultaneous effect of physical influences such as cold, heat and exertion, as well as the consumption of alcohol or the intake of acetylsalicylic acid preparations (favoring the absorption of macromolecules). In addition, an essential prerequisite for allergic reactions is genetic disposition (see “Causes at a Glance” for more information).
“IgE-mediated allergic food hypersensitivity-food allergy.”
In allergic food intolerances mediated by specific immunoglobulins E (IgE) antibodies, the immune system views the proteins or protein cleavage products (allergens) contained in the food as foreign bodies and consequently forms antibodies (sensitization) [1,3]. IgE antibodies are bound on the surface of mast cells and basophilic leukocytes (white blood cells). Re-introduction of the specific antigen leads to an antigen-antibody reaction and thus to activation of basophilic leukocytes and mast cells. As a result, increased mediators, such as histamines, are released from the mast cells, leading to the typical clinical symptoms of an immediate type or type 1 reaction (synonyms: type I allergy, type I immune reaction). In most cases, the symptoms occur within about 30 minutes, sometimes after a few minutes up to 2 hours, after allergen contact. Subsequently, a second phase of the reaction occurs, reaching its maximum after 4 to 6 hours after allergen contact. Major factors influencing oral sensitization with an immediate-type allergic reaction:
- Genetic predisposition of the individual.
- Amount and potency of the allergen
- Impaired function of the gastrointestinal mucosal barrier (due to dysbiosis).
- Age
Non-IgE-mediated allergic food hypersensitivity
Food allergies, unlike IgE antibodies, can rarely be mediated by specific immune cells. In the so-called type 4 reaction (synonyms: type IV allergy, late-type allergic reaction), the immune response – T lymphocytes reacting with the allergen – occurs with a delay. This explains why, in some sufferers, symptoms do not appear until several hours to three days after eating the allergenic food. The mechanism of origin of non-IgE antibody-mediated hypersensitivities is currently unknown. However, studies in children with atopic eczema (neurodermatitis) have shown that a combination of IgE- and T-cell-mediated responses may be important for the pathomechanism. For example, allergic contact dermatitis represents a T-lymphocyte mediated disease. The T-lymphocytes react as a hapten-protein complex with low molecular weight substances such as nickel or chromium. In persons who have been sensitized with nickel for a long time and very strongly, the oral intake of this classical allergen with food can lead to a hematogenous contact eczema – depending on the dose.Based on the sensitization pathway and the type of allergens involved, three types of food allergy are distinguished:
| Food allergies type A | Food allergies type B | Food allergies type C | |
| Affected | Infants and young children | Older children, adolescents and adults | especially women |
| Atopic disposition | Present | present | often none |
| Sensitization pathway | Via the gastrointestinal tract | Aerogenic sensitization to pollen or occupational allergens; course: clinically manifest or subclinical; bypasses oral tolerance to foods such as vegetables nuts, fruits, etc., that contain similar proteins (cross-reactivity) | Via the gastrointestinal tract |
| Trigger of the complaints | Relatively stable proteins, which often disappear when oral tolerance matures | Heat-stable food allergens that induce direct sensitization by the aerogenic route | Few, relatively stable food proteins |
| Affected foods | Especially milk, egg, cereal, soy, fish, peanut, | especially fruit, vegetables, nuts |
Etiology (causes)
Biographical causes
- Genetic exposure through parents, grandparents A major prerequisite for allergic reactions is genetic disposition:
- The risk of expressing allergic symptoms is 5-15% if neither parent is atopic
- The risk of developing allergy is 20-40% if one parent has a predisposition to allergies
- The risk of expression of allergic symptoms is 40-60% if both parents suffer from atopic disease
- The risk of expression of allergic symptoms increases to 60-80% if both parents have the same allergic manifestation
- Genetic risk dependent on gene polymorphisms:
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
- Genes: HLA-DRA
- SNP: rs7192 in the gene HLA-DRA
- Allele constellation: GT (1.7-fold risk of developing peanut allergy).
- Allele constellation: TT (3.0-fold risk of developing peanut allergy).
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
Behavioral causes
- Nutrition
- Unilateral overeating
- Spices – substance that promotes absorption.
- Consumption of stimulants
- Women who do not breastfeed their newborn children.
- Inhalation of allergens such as house dust or animal dander.
Disease-related causes
- Allergies such as birch pollen allergy or allergic bronchial asthma.
